The shedding of NKG2DLs, mediated by tumor-secreted metalloproteases or the release of NKG2DLs via exosomes, leads to soluble MICA/B that can bind to NKG2D receptors thereby impairing the effector functions of NK and T cell that rely on NKG2D signaling (39). This evidence concerns the gene KLRK1 and neoplasm.